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Prevention of headaches via avoidance of triggers remains the main behavioral treatment suggestion for headache management despite trigger avoidance resulting in increases in potency, lifestyle restrictions, internal locus of control decreases, pain exacerbation and maintenance. New approaches, such as Acceptance and Commitment Therapy (ACT), instead emphasize acceptance and valued living as alternatives to avoidance. Though ACT is an empirically supported treatment for chronic pain, there is limited evidence for headache management whilst preliminary outcome studies are afflicted with methodological limitations. This study compared an ACT-based group headache-specific intervention to wait-list control, in a randomized clinical trial, on disability, distress, medical utilization, functioning and quality of life. 94 individuals with primary headache (84% women; Mage=43 years; 87.35% migraine diagnosis) were randomized into two groups (47 in each). Assessments occurred: before, immediately after, and at 3-months following treatment end. Only the ACT group was additionally assessed at 6- and 12-months follow-up. Results (intent to treat analyses corroborated by linear-mixed-model analyses) showed substantial improvements in favor of ACT compared to control, on disability, quality of life, functional status, and depression at 3-, 6-, and 12-month follow-up. Improvements were maintained in the ACT group at 6- and 12-month follow-up. At 3-month follow-up, clinical improvement occurred in headache-related disability (63%) and 65% in quality of life in ACT vs. 37% & 35% in control. These findings offer new evidence for the utility and efficacy of ACT in localized pain conditions and yields evidence for both statistical and clinical improvements over a years' period. Perspective: An Acceptance and Commitment Therapy approach focusing on acceptance and values-based activities, was found to improve disability, functioning and quality of life among patients with primary headaches. Trial registration: Clinical trials.gov registry (NCT02734992).
The measurement of pain in animals is surprisingly complex, and remains a critical issue in veterinary care and biomedical research. Based on the known utility of pain measurement via facial expression in verbal and especially non-verbal human populations, "grimace scales" were first developed a decade ago for use in rodents and now exist for 10 different mammalian species. This review details the background context, historical development, features (including duration), psychometric properties, modulatory factors, and impact of animal grimace scales for pain.
To determine whether training with a brain-computer interface (BCI) to control an image of a phantom hand, which moves based on cortical currents estimated from magnetoencephalographic signals, reduces phantom limb pain.
Although convincing experimental evidence indicates that Na/K/Cl cotransporter 1 (NKCC1) is involved in spinal nociceptive information processing and in the generation of hyperalgesia and allodynia in chronic pain states, the cellular distribution of NKCC1 in the superficial spinal dorsal horn is still poorly understood. Because this important piece of knowledge is missing, the effect of NKCC1 on pain processing is still open to conflicting interpretations. In this study, to provide the missing experimental data, we investigated the cellular distribution of NKCC1 in the superficial spinal dorsal horn by immunohistochemical methods. We demonstrated for the first time that almost all spinal axon terminals of peptidergic nociceptive primary afferents express NKCC1. In contrast, virtually all spinal axon terminals of nonpeptidergic nociceptive primary afferents were negative for NKCC1. Data on the colocalization of NKCC1 with axonal and glial markers indicated that it is almost exclusively expressed by axon terminals and glial cells in laminae I-IIo. In lamina IIi, however, we observed a strong immunostaining for NKCC1 also in the dendrites and cell bodies of PV-containing inhibitory neurons and a weak staining in PKCγ-containing excitatory neurons. Our results facilitate further thinking about the role of NKCC1 in spinal pain processing.
Osteoarthritis is a mechanical abnormality characterized by chronic joint pain associated with degeneration of the articular cartilage, synovitis, and local inflammation, leading to loss of function and pain. A connection exists between the peripheral nervous system and inflammatory joint degeneration. The process by which inflammation is influenced by the nervous system is known as neuroinflammation. One of the neuropeptides involved in peripheral neuroinflammation is nociceptin, a peptide related to the opioid class of substances. Nociceptin has both pro- and anti-inflammatory effects. Some studies show that nociceptin can be measured in synovial fluid, while other studies have not been able to detect it. The presence of nociceptin in synovial fluid could imply a molecular role for the neuropeptide in the joint, both physiologically as well as pathophysiologically. The goal of this pilot study was to determine whether nociceptin was present in the synovial fluid of osteoarthritic knees.
Previous studies of herpes zoster (HZ) have focused on acute patient manifestations and the most common sequela, postherpetic neuralgia (PHN), both serving to disrupt brain dynamics. Although the majority of such patients gradually recover, without lingering severe pain, little is known about life situations of those who recuperate or the brain dynamics. Our goal was to determine whether default mode network (DMN) dynamics of the recuperative population normalize to the level of healthy individuals.
The delta opioid receptor (DOR) has been identified as a therapeutic target for migraine, with DOR agonists exhibiting low abuse potential compared with conventional µ-opioid agonists. TRV250 is a novel small molecule agonist of the DOR that is preferentially selective for G-protein signaling, with relatively little activation of the β-arrestin2 post-receptor signaling pathway. This selectivity provides reduced susceptibility to proconvulsant activity seen with non-selective DOR agonists. TRV250 significantly reduced nitroglycerin-evoked hyperalgesia in rodents, indicating a potential utility in acute migraine without the risk of seizure activity or abuse potential.
The aim of this scoping review was to identify initiatives focused on the secondary prevention and management of chronic pain in Australian primary care to understand options available to Primary Health Networks and to identify evidence gaps. The Medline, EMBASE, Cumulative Index to Nursing and Allied Health Literature and Cochrane databases, as well as relevant websites, were searched for eligible records published from 2007 to 2018. Initiative characteristics and outcomes evaluated were extracted and synthesised. In all, 84 initiatives from 167 published and grey literature records were identified, including: (1) consumer initiatives that aimed to improve access to multidisciplinary care, health literacy and care navigation (n=56); (2) health professional capacity building initiatives that aimed to ensure health professionals are skilled and provide best-practice evidence-based care (n=21); and (3) quality improvement and health system support initiatives (n=7). Evidence gaps were found relating to initiatives addressing the secondary prevention of chronic pain, those targeting vulnerable and regional populations, health professional capacity building initiatives for all primary health care providers and quality improvement and system support initiatives. Addressing evidence gaps related to effectiveness, cost-effectiveness and implementation should be the focus for future chronic pain initiatives in primary care settings.
CGRP Antibodies are high-cost newly licensed migraine preventatives.
Cortical spreading depression (CSD) is the propagation of a relatively slow wave in cortical brain tissue that is linked to a number of pathological conditions such as stroke and migraine. Most of the existing literature investigates the dynamics of short term phenomena such as the depolarization and repolarization of membrane potentials or large ion shifts. Here, we focus on the clinically-relevant hour-long state of neurovascular malfunction in the wake of CSDs. This dysfunctional state involves widespread vasoconstriction and a general disruption of neurovascular coupling. We demonstrate, using a mathematical model, that dissolution of calcium that has aggregated within the mitochondria of vascular smooth muscle cells can drive an hour-long disruption. We model the rate of calcium clearance as well as the dynamical implications on overall blood flow. Based on reaction stoichiometry, we quantify a possible impact of calcium phosphate dissolution on the maintenance of F0F1-ATP synthase activity.